Study On Cognitive Deficits After Traumatic Brain Injury In Rats

Objective With the development of national economy and traffic, the incidence of brain injury and the injured disabled has been increased year by year,and the learning and memory disable is one of the most durable and serious symptoms, particularly in relation to the diminished ability for learning new knowledge. The study of the TBI mechanism of cognitive impairment, mainly focused on the role of cholinergic system studies. However, other neurotransmitters and molecules are not reported yet. This study is to detect the changes of the content of the acetylcholine and the neural cell adhesion factor ,and preliminary study the relationship between them and cognitive impairment after TBIMethods Brain injury model of SD rat is made through the weight falling fight the brain . According to the different of intensity to clampdown ,rats are divided into mild, moderate and sham group, and tested the levels of acetylcholine transferase and neural cell adhesion factor at different time points .Finally, understand the changing trend of acetylcholine transferase and neural cell adhesion factor in the different degrees of injury through to analyze the data.Results After brain damage , the acetylcholin transferase's content compares the control group to drop, and Data change imply the tendency which firsts rise then fall; The mild group declining trend is weak,and replies quickly. The change of the neural cell adhesion factor content also assumes firsts rise then fall. The discovery in the 7th day find the content surpass the control group obviously. The tendency of Two different factors is adopt to the change of cognitive impairment by water maze test after injury.Conclusion (1)There are significantly changes in the ChAT and NCAM expression of prefrontal lobe , hippocampus, basal forebrain after TBI , and the changes of the moderate damage group is more than the mild damage group .(2 ) The tedency of ChAT content is similary to the NCAM after TBI. (3 ) The changes of ChAT and NCAM correlate with cognitive deficits after TBI.